Numerous types of devices and systems exist today that monitor and treat abnormal behavior of the heart (arrhythmias). Examples of arrhythmias include tachycardia, fibrillation and the like. With normal conduction, the cardiac contractions are very organized and timed so that the top chambers (the atria) contract before the lower chambers and the heart rate is maintained between 60 and 120 beats per minute. Fast, abnormal heart rhythms are called tachyarrhythmias. Ventricular tachycardia (VT) is a tachyarrhythmia that originates in the ventricle and may be life-threatening. Symptoms of VT include feeling faint, sometimes passing out, dizziness, or a pounding in the chest.
Supraventricular tachycardia (SVT) refers to a rapid heart rhythm originating above the ventricular tissue. Supraventricular tachycardias can be contrasted to ventricular tachycardias—rapid rhythms that originate within the ventricular tissue. Although an SVT can be due to any supraventricular cause, the term is often used to refer to one specific cause of SVT, namely Paroxysmal supraventricular tachycardia (PSVT) which is due to AV nodal reentrant tachycardia.
Tachycardias can result due to any number of reasons. For example, patients who have had myocardial infarctions, or other diseases that create scarring in the ventricular region of the heart, often develop monomorphic ventricular tachycardias. A monomorphic ventricular tachycardia (MVT) is a type of tachycardia that originates from one ventricular focus. These tachycardias often arise in and around an area of scarring on the heart. They are typically uniform and typically occur at a regular rate. Faster MVTs are often associated with hemodynamic compromise, whereas slower MVTs can be very stable.
SVTs and VTs may be treated with medication, catheter ablation, surgery, and an implantable medical device (IMD). The IMD may treat VT or SVT by pacing the heart, such as antitachycardia pacing (ATP) or, when ATP does not terminate the arrhythmia, delivering a high voltage shock to terminate the arrhythmia.
Numerous conventional algorithms exist to discriminate VT and SVT through passive approaches. These passive algorithms discriminate between different arrhythmias based on the morphology of one or more prior cardiac beats or events/cycles. The conventional passive algorithms also utilize one or more prior cardiac events/cycles to determine physiologic behavior such as the RR interval, AR interval, EGM width, RR regularity, onset, and morphology (bipolar and far-field) and the like.
However, conventional passive rhythm discrimination methods have experienced certain limitations. For example, conventional passive rhythm discrimination methods may be unable to differentiate between VT and SVT. Further, poly-morphic VT may be irregular which in turn leads to mischaracterization by certain passive rhythm discrimination methods. Also, passive rhythm discrimination methods may be susceptible to variation in variables associated with the IMD electronics, such as conduction aberrance, signal truncation or misalignment, saturation of electrodes after shocks and the like.
Various passive rhythm discrimination implementations are used today, each of which affords different sensitivity and specificities. For example, different manufactures use different morphology methods (e.g., alignment of peaks in cardiac events, use of wavelets, and the like). The accuracy of these methods depends on multiple variables, such as signal mismatch. Signal mismatch may be caused by signal truncations, position of the starting points, and near field sensitivity. Some passive rhythm discrimination methods store templates that may also be somewhat different from the real time signals. The differences between templates and real signals may lead to mischaracterization, and different levels of sensitivity and specificity.
More recently, it has been proposed to utilize an active discrimination method which involves, upon detecting an arrhythmia, immediately delivering an anti-tachy pacing (ATP) therapy to the right atrium (RA) and the right ventricle (RV). The ATP therapy is delivered without delay as soon as an arrhythmia is detected. The active discrimination method then determines whether the arrhythmia persists. If the arrhythmia persists, then the first returned beat is considered the origin of the arrhythmia. When the arrhythmia persists, the active discrimination method next determines which chamber exhibits the first returned beat, namely the chamber in which the next cardiac cycle begin. If the first returned beat originates in the RA, the arrhythmia is declared to be a SVT. If the first returned beat originates in the RV, the arrhythmia is declared to be a VT.
However, this active discrimination method experiences certain limitations. For example, a post ventricular contract (PVC) or a post atrial contraction (PAC) may cause mischaracterization of an arrhythmia. Also, in certain instances, the heart may experience oscillations or aberrations at the end of an ATP therapy. When PVC, PAC, oscillation or aberration occurs, a risk exists that the PVC, PAC, oscillation or aberration may cause the arrhythmia to be mischaracterized as VT when the arrhythmia is in fact SVT, or mischaracterized as SVT when the arrhythmia is in fact VT.